Why the study?
SARS-CoV-2 can cause fatal cardiovascular events and multiple organ damage through vascular impairment, making it pivotal to elucidate the mechanisms by which the virus causes endothelial and vascular dysfunction.
This review highlights the critical role of endothelial infection and ACE2 inhibition in driving vascular dysfunction and cardiovascular complications during acute COVID-19.
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May warrant CV vigilance in COVID-19; leaves open mechanistic targets for prospective trials.
The cumulative number of cases in the current global coronavirus disease 19 (COVID-19) pandemic, caused by the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has exceeded 100 million, with the number of deaths caused by the infection having exceeded 2.5 million. Recent reports from most frontline researchers have revealed that SARS-CoV-2 can also cause fatal non-respiratory conditions, such as fatal cardiovascular events. One of the important mechanisms underlying the multiple organ damage that is now known to occur during the acute phase of SARS-CoV-2 infection is impairment of vascular function associated with inhibition of angiotensin-converting enzyme 2. To manage the risk of vascular dysfunction-related complications in patients with COVID-19, it would be pivotal to clearly elucidate the precise mechanisms by which SARS-CoV-2 infects endothelial cells to cause vascular dysfunction. In this review, we summarize the current state of knowledge about the mechanisms involved in the development of vascular dysfunction in the acute phase of COVID-19.
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Nakano et al. (2021) studied this question.
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